Drugs that activate this novel stress response pathway, which they call the mitochondrial-to-cytosolic stress response, protected both nematodes and cultured human cells with Huntington´s disease from protein-folding damage.
Reporter: Aviva Lev-Ari, PhD, RN
“Maybe there is a way to use one drug to alter the mitochondrial signal and another drug to alter the communciation signal from the brain,” he said. “You would never see these two effects if you were studying protein folding in a tissue culture dish, because you don’t have the whole organism, C. elegans, in which you can look at the signals being communicated.”
Co-authors of the fat study include Hyun-Eui Kim, Ana Rodrigues Grant, Milos Simic, Rebecca Kohnz, Daniel Nomura, Jenni Durieux, Celine Riera, Melissa Sanchez, Erik Kapernick and Suzanne Wolff at UC Berkeley. The second study was co-authored by Kristen Berendzen, Jenni Durieux, Ye Tian, Hyun-eui Kim and Suzanne Wolff of UC Berkeley, in collaboration with Li-Wa Shao and Ying Liu of Peking University in Beijing.
The studies are supported by the Howard Hughes Medical Institute, National Institutes of Health, Glenn Foundation for Medical Research, and Jane Coffin Childs Memorial Fund for Medical Research.
- Lipid Biosynthesis Coordinates a Mitochondrial-to-Cytosolic Stress Response(Cell)
- Neuroendocrine Coordination of Mitochondrial Stress Signaling and Proteostasis (Cell)
- Andrew Dillin’s lab website